Effects of inhaled nitric oxide at rest and during exercise in idiopathic pulmonary fibrosis

Author:

Blanco Isabel1,Ribas Jesús2,Xaubet Antoni13,Gómez Federico P.13,Roca Josep13,Rodriguez-Roisin Robert13,Barberà Joan A.13

Affiliation:

1. Department of Pulmonary Medicine, Institut Clínic del Tórax, Hospital Clínic-Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, and

2. Hospital Universitari de Bellvitge-IDIBELL, Barcelona; and

3. Centro de Investigación Biomédica en Red de Enfermedades Respiratorias, Buñola, Spain

Abstract

Patients with idiopathic pulmonary fibrosis (IPF) usually develop hypoxemia and pulmonary hypertension when exercising. To what extent endothelium-derived vasodilating agents modify these changes is unknown. The study was aimed to investigate in patients with IPF whether exercise induces changes in plasma levels of endothelium-derived signaling mediators, and to assess the acute effects of inhaled nitric oxide (NO) on pulmonary hemodynamics and gas exchange, at rest and during exercise. We evaluated seven patients with IPF (6 men/1 woman; 57 ± 11 yr; forced vital capacity, 60 ± 13% predicted; carbon monoxide diffusing capacity, 52 ± 10% predicted). Levels of endothelin, 6-keto-prostaglandin-F, thromboxane B2, and nitrates were measured at rest and during submaximal exercise. Pulmonary hemodynamics and gas exchange, including ventilation-perfusion relationships, were assessed breathing ambient air and 40 ppm NO, both at rest and during submaximal exercise. The concentration of thromboxane B2increased during exercise ( P = 0.046), whereas levels of other mediators did not change. The change in 6-keto-prostaglandin-Fcorrelated with that of mean pulmonary arterial pressure ( r = 0.94; P < 0.005). Inhaled NO reduced mean pulmonary arterial pressure at rest (−4.6 ± 2.1 mmHg) and during exercise (−11.7 ± 7.1 mmHg) ( P = 0.001 and P = 0.004, respectively), without altering arterial oxygenation or ventilation-perfusion distributions in any of the study conditions. Alveolar-to-capillary oxygen diffusion limitation, which accounted for the decrease of arterial Po2during exercise, was not modified by NO administration. We conclude that, in IPF, some endothelium-derived signaling molecules may modulate the development of pulmonary hypertension during exercise, and that the administration of inhaled NO reduces pulmonary vascular resistance without disturbing gas exchange.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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